Hydroxyethyl starch reduces the chemotaxis of white cells through endothelial cell monolayers

Citation
R. Hofbauer et al., Hydroxyethyl starch reduces the chemotaxis of white cells through endothelial cell monolayers, TRANSFUSION, 39(3), 1999, pp. 289-294
Citations number
36
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
TRANSFUSION
ISSN journal
00411132 → ACNP
Volume
39
Issue
3
Year of publication
1999
Pages
289 - 294
Database
ISI
SICI code
0041-1132(199903)39:3<289:HSRTCO>2.0.ZU;2-M
Abstract
BACKGROUND: Polymorphonuclear leukocytes (PMNs) play a tremendous role duri ng inflammatory processes. PMNs have to pass a monolayer of endothelial cel ls to migrate into the extravascular space. Hydroxyethyl starch (HES) is fr equently used as a volume expander in critically ill patients. STUDY DESIGN AND METHODS: The aim of this study was to investigate whether HES influences the chemotaxis of PMNs through endothelial cell monolayers b y using a test system that allows the simultaneous treatment of both cell t ypes. Human umbilical endothelial cells were cultured on microporous membra ne filters. PMNs were isolated and PMN chemotaxis was studied. RESULTS: The number of untreated PMNs that migrated through untreated endot helial cell monolayers in response to a chemoattractant was used as a contr ol and set as 100 percent. In clinically relevant concentrations, HES was a ble to significantly decrease PMN chemotaxis through endothelial cell monol ayers, showing a dose-dependent effect (0.1 mg/mL: 99.6 +/- 10.9%, p = NS c ompared to control; 1 mg/mL: 82.4 +/- 8.3%, p<0.05 compared to control; 10 mg/mL: 62.9 +/- 11.7%, p<0.05). In this assay, both cell types (PMNs and en dothelial cells in the monolayer) were treated simultaneously, which simula ted the clinical situation after an intravenous injection of HES. The treat ment of one cell type, PMNs (89.6 +/- 8.8%, p<0.05) or endothelial cells in the monolayer (76.2 +/- 9.4%, p<0.05), suggests that the influence on endo thelial cells is greater. CONCLUSION: HES is able to significantly reduce the chemotaxis of PMNs thro ugh endothelial cell monolayers. The possible clinical consequence of a mod erate reduction in endothelium-mediated PMN chemotaxis in critically ill pa tients remains to be evaluated.